Abstract: PO1741
C5a Enhanced the Recruitment of CD16+ Monocytes by CX3CL1-CX3CR1 Axis in ANCA-Associated Vasculitis
Session Information
- Glomerular Diseases: Vasculitis and TMA
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1202 Glomerular Diseases: Immunology and Inflammation
Authors
- Tang, Jiale, Xiangya Hospital Central South University, Changsha, Hunan, China
- Liao, Zhonghua, Xiangya Hospital Central South University, Changsha, Hunan, China
- Li, Xiaozhao, Xiangya Hospital Central South University, Changsha, Hunan, China
Background
Monocytes play a major role in ANCA-associated glomerulonephritis. The mechanism is not well understood. Additionally, it is a consensus that C5a participates ANCA-associated vasculitis (AVV) pathogenesis. The relevance of C5a in terms of monocytes recruitment, as well as the nature and function of monocytes has not been well studied in AAV.
Methods
Monocytes in blood was counted and its phenotypic characteristics were analyzed by Flow cytometry. C5a and monocyte - related cytokines and chemokines was detected in AAV. The phenotype of monocytes in Kidney tissues from MPO-AVV patients was studied by immunohistochemistry and immunofluorescence. The chemoattractant activity of chemokines produced by human renal glomerular endothelial cells（HRGEC）for monocytes was observed.
Results
Monocytes were higher in activated MPO-AAV patients. The proportion of CD16+ monocytes in the peripheral blood of the patients was significantly reduced and CX3CR1 was highly expressed in CD16+ monocytes. C5a, IL-6, TNF-α, and chemokine CX3CL1 were significantly increased in serum of activated MPO-AAV patients. CD16+ monocytes were clearly seen in the glomeruli of MPO- AVV patients. Chemokine CX3CL1 was expressed in glomerular endothelial cells. Consistently, we demonstrated C5a enhance recruitment of CD16+ monocyte via CX3CL1 produced by TNF-αinduced HRGEC in vitro.
Conclusion
We report an altered distribution of monocyte subsets in MPO-AAV patients; CD16+ monocytes may be recruited to kidney through CX3CL1-CX3CR1 axis to aggravate ANCA-associated GN.